Intracranial aneurysms
and SAH
Philippe Younes MD
Neurosurgeon
Head of Neuroscience department BMC
Subarachnoid hemorrhage(SAH)
Blood in the subarachnoid space,
between arachnoid membrane
and the pia matter
SAH
Post traumatic or spontaneous
Trauma is the most common cause
Most cases of spontaneous SAH are due to aneurysmal rupture
Peak age for aneurysmal SAH is 55–60 years, ≈ 20% of cases occur between
ages 15–45 yrs
30% of aneurysmal SAHs occurs during sleep
Sentinel headaches that precede the SAH-associated ictus have been
reported by 10-50% of Patients and most commonly occur within 2-8 weeks
before overt SAH.
SAH
Headache is lateralized in 30%, most to the side of the aneurysm
SAH is complicated by intracerebral hemorrhage in 20–40%, by
intraventricular hemorrhage in 13–28% and by subdural blood in 2–5%;
usually due to p-comm aneurysm when over convexity, or distal anterior
intracerebral artery (DACA) aneurysm with interhemispheric subdural
Soft evidence suggests that rupture incidence is higher in spring and
autumn
Patients ≥ 70 yrs age have a higher proportion with a severe neurologic
grade
Seizures may occur in up to 20% of patients after SAH, most commonly in
the first 24 hours and are associated with ICH, HTN and aneurysm location
(MCA & acomm)
Outcome of aneurysmal SAH
10–15% of patients die before reaching medical care
Mortality is 10% within first few days
30-day mortality rate was 46% in one series and in others over half the patients
died within 2 weeks of their SAH
Median mortality rate in epidemiological studies from U.S. has been 32% vs. 44%
in Europe and 27% in Japan (may be an underestimate based on
underreported prehospital death)
Causes of mortality
25% die as a result of medical complications of SAH
neurogenic pulmonary edema
neurogenic stunned myocardium
about 8% die from progressive deterioration from the initial hemorrhage
Outcome of aneurysmal SAH
Among patients surviving the initial hemorrhage treated without surgery,
rebleeding is the major cause of morbidity and mortality, the risk is ≈ 15–20%
within 2 weeks. The goal of early surgery is to reduce this risk
Of those reaching neurosurgical care, vasospasm kills 7%, and causes severe
deficit in another 7%
About ≈ 30% of survivors have moderate to severe disability, with rates of
persistent dependence estimated between 8-20% in population based studies
66% of those who have successful aneurysm clipping never return to the same
quality of life as before the SAH
Patients ≥ 70 years age fare worse for each neurologic grade.5 A multivariate
analysis revealed age and WFNS grade to be most predictive of long-term
outcome, regardless of treatment modality
The severity of clinical presentation is the strongest prognostic indicator
Incidence of ASAH
9.7-14.5 per 100000
Increases with age
Higher in woman 1.24 times
Higher in African Americans and Hispanics
Risk Factors
Behavioral
Hypertension, cigarette smoking and alcohol abuse
Females
History of cerebral aneurysm
morphology: bottleneck shape (Saccular) and increased ratio of size of
aneurysm to parent vessel have been associated with increased risk of rupture
Family history of aneurysms (at least 1 first-degree family member and especially
if ≥ 2 are affected)
Genetic syndromes
autosomal dominant polycystic kidney disease
type IV Ehlers-Danlos syndrome
Clinical presentation
Severe headache (worst H/A of my life), of sudden onset
To be differentiated from other severe paroxysmal headache
Crash migraine or benign thunderclap H/A
Reversible cerebral vasoconstriction syndrome (RCVS)
Benign orgasmic chephalgia
Meningismus
HTN
Focal neurologic deficit
DLOC or coma
Aneurysm type
Saccular aneurysms
are by far the most
common type.
Characteristically
occur at branch
points of major
cerebral arteries.
Aneurysm distribution by
location
Aneurysms are frequently
classified according to their
size, with small being smaller
than 10 mm, large being 10 to
25 mm, and giant being larger
than 25 mm.
At presentation, most are small,
with only 2% found to be giant
Giant aneurysms
Giant Aneurysm of Aneurysm of basilar bifurcation
supraclinoidsegment of internal projecting posteriorly, invading
carotid artery elevating optic chiasm, peduncles and compressing cerebral
distorting infundibulumand aqueduct. Corticospinal tracts may
compressing oculomotor(III) nerve be affected, resulting in paralysis or
paresis
it is thought that
intracranial aneurysms
form over a relatively short
period and either rupture
or undergo a stabilizing
change resulting in an
unruptured aneurysm.
Pathologic examination of
ruptured aneurysms
obtained at autopsy
demonstrates loss of the
internal elastic lamina, loss
of the media-SMC
,disorganization of normal
vascular architecture, and
reduced collagen
content.
In contrast, unruptured
aneurysms have nearly
twice the collagen
content of the normal
arterial wall, resulting in
increased thickness of the
aneurysmal wall
Pathophysiology
The volume of blood escaping during aneurysm rupture varies from a negligible amount
that constitutes a “warning leak” to massive amounts (≥150 mL) that are associated with
immediate death.
The pathophysiologic consequences depend on the volume and location of the bleeding
as well as on the preexisting size of the cerebrospinal fluid (CSF) space into which the
aneurysm ruptures and the patient’s age and premorbid condition.
The etiology of increased ICP acutely after SAH includes acute hydrocephalus,
intraventricular hemorrhage (IVH) or intracerebral hemorrhage, brain swelling, ischemic
brain edema, and increased resistance to CSF outflow probably as a result of blockade of
the arachnoid villi by blood. There is some evidence that the blood-brain barrier is
disrupted after SAH, and this could contribute to edema and brain swelling.
Increased ICP was more likely with worsening neurological grade, larger SAH volume, early
hypodensities on computed tomography (CT) scan, and rebleeding.
mean ICP was 10 mm Hg in
patients in Hunt and Hess
clinical grades I and II, 18 mm
Hg in patients in grades II and
III, and 29 mm Hg in patients
in grades III to V
Angiographic vasospasm,
which was more common in
patients with a poor clinical
grade and larger SAH, was
associated with a significant
rise in ICP from a mean of 16
mm Hg in patients without
vasospasm to 29 mm Hg in
those with vasospasm
Pathophysiology
The most common time of development of increased ICP is within 3 to 4
days of SAH. The association of increased ICP, especially when occurring
after several days, should be considered in patients experiencing clinical
deterioration days after SAH, because reducing ICP with external
ventricular drainage (EVD) can substantially improve CPP.
The time course of CBF changes after SAH shows that mean CBF decreases
with time, reaching a nadir 10 to 14 days after SAH, after which CBF slowly
increases toward normal.
The cerebral metabolic rate of oxygen (CMRO2) shows a similar pattern,
with progressive reductions associated with deteriorating clinical grade
and worsening angiographic vasospasm.
Diagnosis
The clinical diagnosis of SAH is best confirmed with brain CT.
CT confirms the SAH and frequently highlights associated issues such as
hydrocephalus, intraparenchymal hematoma, intraventricular hemorrhage,
or subdural hemorrhage.
Sensitivity is highest in the first 24 hours after headache onset. A mild
hemorrhage may wash away within 24 hours.
However, approximately 50% of severe SAHs are still visible on CT 1 week
after the ictus, and almost one third are still seen after 2 weeks
Whenever the clinical suspicion of
SAH exists but CT is negative, a
lumbar puncture must be
performed.
A nontraumatic tap is crucial.
When the presence of blood in the
CSF does not clear between the
first and fourth tubes, this is
particularly suggestive of SAH.
•However, a more sensitive
indicator is CSF xanthochromia,
which represents the lysis of
erythrocytes within the CSF. This
renders the CSF a yellowish color, is
frequently present within 1 to 3
hours after a SAH and often persists
for approximately 2 to 3 weeks.
When an SAH is confirmed by CT or lumbar puncture, the
source of the hemorrhage must be confirmed.
This is best achieved with a 4-vessel cerebral arteriogram. An
aneurysmal source is found in 80% to 85% of these arteriograms
Perimesencephalic Subarachnoid
Hemorrhage
Occur typically in younger males
who are non hypertensive and who
do not look as ill as typical patients
with an aneurysmal SAH.
Although the clinical presentation is
similar to that of an aneurysmal
SAH, symptom onset is more
gradual, and patients generally do
well.
When these patients have a typical
presentation and characteristic CT
findings and a good quality
angiogram that is negative, a
follow-up arteriogram is not always
needed. The entity of brainstem or
perimesencephalic SAH seems to
represent a clinically benign
disorder of unknown cause.
Management
Specific therapeutic issues pertain to aneurysms, primarily securing them to
prevent rebleeding, management of increased intracranial pressure (ICP) and
hydrocephalus, and treatment of cerebral vasospasm.
Rebleeding:
is the major cause of poor outcome after SAH.
The second hemorrhage is associated with a 70% mortality rate.
If untreated, the risk of subsequent aneurysm rupture is approximately 4% in the first 24
hours and 1.5% per subsequent day, leading to an approximately 27% incidence of
subsequent aneurysmal rupture within the first 2 weeks of hemorrhage.
the only definitive prevention is direct obliteration using surgical or endovascular
techniques.
Hydrocephalus:
Up to 25% of patients with SAH develop an associated cerebral edema with
ventriculomegaly secondary to an accompanying acute hydrocephalus,
independent of grading after the aneurysm rupture, that worsens if left
untreated.
external ventricular drainage is recommended in conjunction with early
aneurysm occlusion.
Of patients with acute hydrocephalus who require ventricular drainage,
approximately one half will ultimately require a ventricular-peritoneal shunt.
Vasospasm
Cerebral vasospasm, a poorly understood problem, is the most feared and
difficult issue associated with SAH.
This represents a pathologic change within the cerebral vessels leading to
vascular narrowing with decreased cerebral blood flow and subsequent stroke.
Vasospasm is correlated with poor clinical grade and larger degrees of
hemorrhage.
It is thought that the products of blood decomposition within the CSF spaces
results in an imbalance between vascular relaxing factor and constricting
factors resulting in vessel spasm and narrowing.
Typically, vasospasm develops about the fourth day after SAH and usually
peaks between 7 and 10 days.
Management includes the use of calcium channel blockers such as
nimodipine, decreasing ICP with ventricular drainage, and augmenting
cerebral circulation, achieved with triple-H therapy, consisting of
hypervolemia, hemodilution, and hypertensive therapy.
Occasionally, ischemic deficits continue to develop despite aggressive
triple-H therapy. In this setting, endovascular maneuvers, such as intra-
arterial papaverine or intracranial angioplasty, can be used with excellent
results.
Systemic complications
The massive ICP increase affects the hypothalamus; when combined with the
associated global ischemia, there is a massive neuroendocrine response.
Consequently, there is a catecholamine surge leading to cardiac and
pulmonary injury.
Other patients may present with acute respiratory distress syndrome from
massive pulmonary edema, termed neurogenic pulmonary edema.
There is usually an associated acute hypertension on presentation and a clinical
suspicion that the hypertension may be secondary to the Cushing response
associated with increased ICP.
Cerebral circulation must be maintained.
Management of hypertension in this setting requires treatment of the increased
ICP such as ventricular drainage of the CSF rather than the use of
antihypertensive medications.
Frequently, abnormalities of electrolytes are also noted, particularly
hyponatremia.
Usually associated with a salt wasting state rather than a syndrome of
inappropriate antidiuretic hormone, hyponatremia should be managed
accordingly.
UnrupturedAneurysms
Symptomatic unruptured Asymptomatic
aneurysm unruptured aneurysm
Symptomatic unruptured aneurysms often Truly asymptomatic unruptured aneurysms are less prone
require treatment because the presenting
symptom frequently is the harbinger of an to bleeding than symptomatic unruptured aneurysms.
oncoming bleeding episode.
These lesions are frequently discovered during
Various symptoms can be described, most investigation of other neurologic complaints or screening
from compression of neural structures: of high-risk patients, such as those with a familial history of
Cranial nerve deficits, especially of CN-III, aneurysms, connective tissue disorders, or polycystic
headaches, and eye pain, as well as kidney disease.
hemiparesis or motor deficits from giant
aneurysms. An initially suggested hemorrhage risk of approximately
0.05% per year in patients with aneurysms smaller than 10
Some aneurysms develop intraaneurysmal
thrombosis that may lead to mm has been supplanted via further analysis, with a low
thromboembolic stroke or transient ischemic risk associated with aneurysms smaller than 6 mm.
attacks.
It is recommended that aneurysms larger than 6 mm
should be treated.
Aneurysms smaller than 6mm should be considered for
treatment in patients with a familial history of SAH, patients
who have had SAH associated with a separate aneurysm,
and very young patients for whom the lifetime risk may
become significant.
Surgical treatment
The development of the surgical microscope and microsurgical
instrumentation and the evolution of skull base techniques have
revolutionized treatment of cerebral aneurysms.
Magnification and brilliant illumination of very narrow exposure windows
has allowed the preservation of small perforating vessels that serve as
strategic end arteries of eloquent brain regions that are not visible to the
naked eye.
Endovascular treatment
Advances in the design of micro catheters, embolization devices, and digital
radiographic software have greatly extended the capability of intravascular
navigation and trans vascular catheter-directed therapies.
The new discipline of interventional neuroradiology or endovascular surgery has
emerged.
In many patients, aneurysm endovascular coil occlusion is a valuable
alternative to surgery.
However, endovascular procedures seem to be less successful when the
degree of complete obliteration and recurrence is compared with surgical
procedures.
Complete aneurysm occlusion is achieved in only 50% of cases.
When near-complete occlusions are included, this level increases to 85% to 90%.
A second limitation to endovascular procedures is aneurysm recurrence;
approximately 16% to 32% of these aneurysms can recur, depending on the
location, degree of compaction, and morphology of the aneurysm when
primarily treated.
Patients may require repeated treatment or even surgical treatment with
removal of the coils.
Procedural morbidity ranges between 6% and 19%. Overall, 82% of patients
experience favorable outcomes.
Team work
Collaboration between neurosurgeons and interventional neuroradiologists will
increase the number of patients who can be safely treated with either
technique or after one technique fails.
The value of this collaborative effort cannot be overemphasized, particularly
with the more complex aneurysms and those within the posterior circulation.
The 2 techniques complement each other. In some instances, the primary
treatment may be coiling.
Others require surgical obliteration, and some aneurysms, because of their
complex structures, giant size, or involvement of critical perforating branches,
are not amenable to either treatment but require combined
neurosurgical/neuroendovascular skills to achieve treatment success.
Thank You
